Corrado Magnino

Echocardiographic Indexes for the Non-Invasive Evaluation of Pulmonary Hemodynamics

Ultrasound imaging has continuously developed over recent years, leading to the development of several novel echocardiographic indexes. Among these, of particular interest are those that focus on pulmonary hemodynamics, because they not only improve both sensitivity and specificity in the echocardiographic evaluation of pulmonary pressures (systolic, mean, and diastolic), but can also be used to estimate other pulmonary hemodynamic parameters, such as pulmonary vascular resistance, pulmonary capillary wedge pressure, and pulmonary capacitance and impedance. Such parameters can provide important diagnostic and prognostic information in patients with heart failure, chronic obstructive pulmonary disease, and pulmonary arterial hypertension and in every patient with suspected pulmonary impairment. In this review, the authors present a comprehensive overview of the echocardiographic indexes involved in pulmonary hemodynamic evaluation and discuss the applications of these indexes in the clinical setting.

Orthostatic hypotension: evaluation and treatment.

Orthostatic hypotension (OH) may be dependent upon various neurogenic and non-neurogenic disorders and conditions. Neurogenic causes include the main autonomic failure syndromes, primary (multiple system atrophy, pure autonomic failure, and autonomic failure associated with Parkinsons disease) and secondary (central nervous system diseases, peripheral neuropathies and systemic diseases). Non-neurogenic causes of OH include cardiac impairment, fluid and electrolyte loss, vasodilatation, and old age. A number of drugs may also cause OH, through their vasoactive action or by interfering with the autonomic nervous system. Symptoms of OH are debilitating, often confining patients to bed, and longitudinal studies have shown that OH increases the risk of stroke, myocardial ischemia and mortality. The therapeutic goal is to decrease the incidence and severity of postural symptoms, rather than restore normotension. In non-neurogenic OH, treatment of the underlying cause may be curative. In neurogenic OH a combination of non-pharmacological and pharmacological measures is often needed. Patient education and non-pharmacological measures represent the first step; among these interventions, fluid repletion and physical countermanoeuvres have been proven very effective. Pharmacological treatment comprises a number of agents acting on blood vessels, on blood volume or with other pressor mechanisms. The drugs most currently used are fludrocortisone and midodrine. Fludrocortisone expands the extravascular body fluid volume and improves alpha-adrenergic sensitivity. Midodrine is a peripheral, selective alpha1-adrenergic agonist that causes arterial and venous vasoconstriction. Despite the wide use of these drugs, multicentre, randomised and controlled studies for the treatment of OH are still scarce and limited to few agents and groups of patients. Pharmacological management of OH substantially improves the quality of life of patients, although it may be problematic. The development of supine hypertension and subsequent congestive heart failure should be avoided, especially in those patients with a pre-existing cardiovascular risk, such as in diabetes or ischemic heart disease.

Ascending aortic dilatation, arterial stiffness and cardiac organ damage in essential hypertension.

Objectives: The objectives of this study were to evaluate the prevalence of dilatation of proximal ascending aorta (pAA) in essential hypertensive patients and the association between pAA dilatation, arterial stiffness and left ventricular hypertrophy. Background: Few data are available regarding patients with pAA dilatation in arterial hypertension. It is not known whether pAA dilatation may be related to increased left ventricular mass and what the relation with central hemodynamics and arterial stiffness would be. Methods: A total of 345 untreated and treated essential hypertensive patients (mean age, 54.3 ± 11 years) were considered for this analysis. We measured pulsatile hemodynamic parameters directly using tonometry, and the proximal aortic diameters through ultrasound imaging (echocardiography). Results: Prevalence of pAA dilatation was 17%. Peripheral hemodynamic parameters were similar in patients with and without ascending aorta dilatation. We observed a slight increase of central systolic (129.81 ± 15.4 vs. 125.02 ± 14.7 mmHg; P = 0.02) and pulse pressure (45.02 ± 10.4 vs. 42 ± 9.54 mmHg; P = 0.02) in patients with pAA dilatation. Pulse wave velocity (9.26 ± 2.33 vs. 7.70 ± 1.69 m/s; P < 0.0001), as well as the augmentation index (25.86 ± 10.2 vs. 19.41 ± 9.52%; P < 0.0001), was significantly greater in patients with pAA dilatation. Finally, left ventricular hypertrophy was thrice as frequent (32.8 vs. 13.4%; P < 0.0001) compared to hypertensive patients without aortic dilatation. Conclusion: This study shows a high prevalence (17%) of ascending aortic dilatation in patients affected by essential hypertension, without further complications. Dilatation of the ascending aorta is associated both to an increased left ventricular mass and arterial stiffness.

Aortic root dilatation in essential hypertension: prevalence according to new reference values.

Background: Aortic root dilatation (ARD) and arterial hypertension represent two important risk factors for aortic dissection: prevalence of observed ARD is increasing – up to 12% in the latest available reports. A recently published work tested on a good number of healthy individuals new reference ranges for aortic root dimensions, suggesting new reference values with corrections for age, gender, height (pHeight) or body surface area (pBSA). Aim: The aim of the study was to evaluate the prevalence of ARD in hypertensive patients using various criteria. Methods: A total of 1076 untreated and treated essential hypertensive patients (mean age, 52.5 ± 2 years) were considered for this analysis. We measured proximal aortic diameters using ultrasound imaging (echocardiography). ARD was defined in three ways. First, when the observed aortic diameter was larger than that predicted for age, sex, and BSA (pBSA), second when larger than predicted by height (pHeight), and third when the aortic diameter to BSA ratio (ASi) was at least 2.1 cm/m2. Results: A total of 237 patients (22% of the study population) showed at least one among the three different criteria defining aortic dilatation. Prevalence of ARD, considering singularly each one of the criteria, varied between 12.8% (pBSA) and 16.9% (pHeight). Conclusion: Our study demonstrated a prevalence of ARD higher than previously reported. Our data suggest, therefore, the necessity of a correct choice of the diagnostic criterion that has to be applied in the single patient for definition of ARD. In particular, using the criterion pHeight in obese patients, we may avoid underdiagnosis of this condition.

Aortic size index enlargement is associated with central hemodynamics in essential hypertension.

The aim of this study was to evaluate the association between brachial and central blood pressure (bBP and cBP) levels and aortic root dilatation (ARD) in essential hypertensive patients. A total of 190 untreated and treated essential hypertensive patients (mean age, 55±11 years) were considered for this analysis. We measured pulsatile hemodynamics and the proximal aortic diameter directly using tonometry, ultrasound imaging (echocardiography) and Doppler. Ninety-one hypertensive patients had an ARD (defined as aortic size index (ASi)>2 cm/m2). Central hemodynamic variables were significantly associated with ASi. Patients with increased ASi were significantly older (60±10 vs. 50±11 years, P<0.0001) and had higher levels of the augmentation index (AIx; 28±10 vs. 21±10 P<0.0001), augmentation pressure (AP; 13±6 vs. 8±5 mm Hg, P<0.0001), and central pulse pressure (cPP; 44±10 vs. 39±8 mm Hg, P<0.0001) compared with patients with normal ASi. In a logistic regression analysis, the AIx was the only significant predictor of ASi. In hypertensive patients, the AIx and cBP were associated with ARD, whereas the bBP was not. Patients with an increased ASi may lose part of the elastic properties of the aorta, demonstrating a strict correlation between ASi and central hemodynamic indexes, in particular, the cPP and AIx.

Left atrial enlargement in essential hypertension: Role in the assessment of subclinical hypertensive heart disease

Abstract Background. Arterial hypertension is a common cause of cardiac organ damage, inducing morphofunctional modifications involving left chambers. This is a retrospective study: it was designed to evaluate the additive clinical value of left atrial enlargement (LAe) assessment in the evaluation of cardiac organ damage. Methods. A total of 814 (67% male; aged 50.7 ± 12 years, mean ± SD) essential hypertensive subjects underwent routinely to a complete and extensive clinical and echocardiographic evaluation. Left ventricular morphology, systolic and diastolic function and left atrial dimension (LAD; linear and volumetric) were evaluated. Results. Prevalence of LAe varied between 6.2% and 52.1%, depending on the chosen criteria (left atrial diameter indexed for body surface area (BSA) vs left atrial volume (LAV) indexed for BSA – LAVi). LAVi showed to be the most sensitive parameter in order to detect it (sensitivity 96%, specificity 100%). Left ventricular hypertrophy (LVH) was present in about one fifth of our population (14% and 26%, considering indexation for BSA and for height2.7). Concentric remodelling (CR) was present in 27–35% of cases considering left ventricular mass indexation for BSA and for height2.7, respectively. In one quarter of our population, LAe was the only echocardiographic sign of hypertension, independent of LVH and CR. Conclusions. LAV evaluation in hypertensive population can contribute to the identification of subjects affected by hypertensive heart disease other than the conventionally evaluated terms (LVH and CR).

Left Heart Morphology and Function in Primary Aldosteronism

Primary aldosteronism is the most frequent cause of secondary hypertension, accounting for up to 11% of cases in selected populations. Patients affected by primary aldosteronism have shown higher prevalence of cardiovascular and cerebrovascular events compared with patients with essential hypertension, despite similar blood pressure levels. Several studies have been performed over past years aiming to explain these data; many of these evaluated echocardiographic differences in hypertension-related cardiac organ damage between primary aldosteronism and essential hypertension. This article summarizes the present knowledge about structural and functional alteration of the human left heart in primary aldosteronism.

Echocardiographic Abnormalities in the Assessment of Cardiac Organ Damage in Never-Treated Hypertensive Patients

Hypertension-related cardiac organ damage, other than left ventricular (LV) hypertrophy (LVH), has been described: in particular, concentric remodeling, LV diastolic dysfunction (DD), and left atrial (LA) enlargement are significantly associated with cardiovascular morbility and mortality in different populations. This study evaluated the prevalence of these latter morphofunctional abnormalities, in never-treated essential hypertensive patients and the role of such a serial assessment of hypertensive cardiac damage in improving cardiovascular risk stratification in these patients. A total of 100 never-treated essential hypertensive subjects underwent a complete clinical and echocardiographic evaluation. Left ventricular morphology, systolic and diastolic function, and LA dimension (linear and volume) were evaluated by echocardiography. Left ventricular hypertrophy was present in 14% of the patients, whereas concentric remodeling was present in 25% of the subjects. Among patients free from LV morphology abnormalities, the most frequent abnormality was LA enlargement (global prevalence 57%); the percentage of patients with at least one parameter consistent with DD was 22% in the entire population, but DD was present as the only cardiac abnormality in 1% of our patient. Left atrial volume indexed for body surface area was the most sensitive parameter in identifying hypertension-related cardiac modification. The global prevalence of cardiac alteration reached 73% in never-treated hypertensive patients. Left ventricular remodeling and LA enlargement evaluation may grant a better assessment of cardiac organ damage and cardiovascular risk stratification of hypertensive patients without evidence of LVH after routine examination.

Inaccuracy of Right Atrial Pressure Estimates Through Inferior Vena Cava Indices

The precision of echocardiography in estimating pulmonary pressures has been debated. A value of right atrial pressure (RAP) is needed for pulmonary pressure estimation, and it could be partly responsible for the estimation error. Several schemes based on the inferior vena cava (IVC) are commonly used in clinical practice and in experimental studies for RAP estimation. However, the majority lack proper validation, and thus far, no study has compared them all. In this prospective, blinded study, a comprehensive transthoracic echocardiography was performed on 200 patients referred for right heart catheterization. The IVC was measured in different views and RAP was estimated according to 6 different schemes. One hundred ninety patients were suitable for analysis. IVC measurements were significantly but poorly associated with invasive RAP. All RAP schemes showed poor accuracy compared with invasive RAP (average accuracy 34%). None of the schemes showed a clear superiority over the others. No echocardiographic or clinical variables showed a relevant impact on the estimation error. In conclusion, RAP estimation based on the IVC is highly inaccurate irrespective of the method used and should be avoided whenever possible. Whether adding estimated RAP values affects the estimation of pulmonary pressures is yet to be determined.

Improving echocardiographic estimation of pulmonary vascular resistance

To the Editor We appreciate the study by Dahiya et al , attempting to improve non-invasive estimation of pulmonary vascular resistance (PVR).1 However, some points deserve a few comments. (1) The new formula (PVRc) compared with the previous one by Abbas et al 2 (PVRe) includes E/e′ ratio, in order to take into account the pulmonary capillary wedge pressure and estimate transpulmonary gradient better. E/e′ is a …